Neoplasms are recognized as foreign tissue and induce an immune response. During induction of tumor immunity, specific T-cells recognizing tumor antigens are stimulated to proliferate and form cytotoxic lymphocytes. Humoral antibodies, secreted by B cells exist concomitantly with the cellular immune response. These immunological responses however, do not appear to proceed in a concerted effort to eradicate the neoplasm. A third parameter, heretofore not considered, is the role tumor cell physiology plays in shielding its destruction by the lymphoid system. Recent studies have suggested that antibody interaction with mammalian cell surfaces causes defoliation of surface antigens. In some instances increased synthesis and secretion of tumor antigens in the presence of an ongoig immune response has been observed. The goal of this investigation will be to delineate the dynamic interaction between tumor cells, lymphoid cells, antibody, and tumor cells. For this goal, antimastocytoma specific antibodies will be prepared and labelled with I125. Tracking of these antibodies on the cell surface will determine whether or not release occurs. In vitro development of tumor immunity will be investigated. The role of the antibody, B-cell, T-cell, and tumor cell physiology will be quantitated. Pharmacological agents which initiate tumor regression will be characterized with respect to their ability to enhance lymphocyte mediated cytotoxicity against mastocytoma cells.